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KATHLEEN E. ROBERTS, MD

Arch Intern Med. 1963;112(2):154-157.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

It is well established that the ingestion of alcohol is followed by a substantial diuresis.¹ If sufficient alcohol is ingested, the diuresis occurs at the expense of all cellular components, and dehydration ensues. One explanation is that alcohol, or one of its metabolites, could be sufficiently small in size so as to be filtered at the renal glomerulus, and if renal tubular reabsorption were sluggish, it could be excreted in the urine and would cause an osmotic type of diuresis.

On the other hand, it has been postulated that alcohol inhibits the release of antidiuretic hormone "per se" and that the inhibition is sufficient to be the entire basis for diuresis. If this hypothesis is true, the osmotic concentration of the urine should decrease coincidentally to an increase in plasma osmotic pressure. In favor of this hypothesis is the finding that hypertonic saline given simultaneously prevents the diuretic effect of . . . [Full Text PDF of this Article]

Author Affiliations
SAN FRANCISCO

Associate Clinical Professor of Medicine, Stanford University School of Medicine, and Director of Research, Roberts Foundation and Clinic.

From the Department of Medicine and Clinical Physiology, St. Mary's Hospital.

Footnotes
Received for publication Oct 10, 1962; accepted Feb 1, 1963.

Supported by USPHS grants H-4449 and A-5356.

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